AIM: To explore the relationship between the alteration in gene expression of sarcoplasmic reticulum Ca~(2+)-ATPase (SERCA) and phospholamban (PLB) in spontaneously hypertensive rats (SHR). METHODS: 294 samples of total RNA were obtained from the tissue of ventriculum , aortic smooth muscle, liver and kidney in SHR and normotensive rats (WKY). RNA array was used to determine the mRNA levels of SERCA and PLB. RESULTS: Compared with age-matched WKY rats, the systolic blood pressure increased higher in 6-week-old SHR (P

Objective CR's advantages of flexibility are analysed, and its reasonable clinical use are evaluated. Methods To compare CR and general roentgenography. Results CR system is one of main X-ray photography. Conclusion Because of the unique advantages of CR, CR and DR will be still clinically equally important in the future for a long period of time.

AIM: The purpose of this study was to determine whether the signal transduction systems were activated at the molecular atrial tissue level in patients with atrial fibrillation (AF) and whether atrial expression of extracellular-signal regulated kinase (ERK) and protein phosphatases is altered. METHODS: Atrial tissue sample of 30 patients undergoing cardiac surgery were examined. 20 patients had AF, 10 patients had no history of AF. The mRNA expression of calcineurin B and MKP-1 were detected by semi-quantitative RT-PCR. ERK1 and phospho-ERK1 were analyzed at the protein level by Western blot. RESULTS: Western blot analysis showed that atrial fibrillation did not induce significant change in ERK1 expression level in the left atrium. In contrast , phospho-ERK1 content was increased in the patients with AF in comparison with those who had sinus rhythm (SR). The mRNA expression of calcineurin B and MKP-1 in the patients with AF were significantly higher than that in patients with SR. CONCLUSION: The activation of extracellular-signal regulated kinase and protein phosphatases may have correlation with the initiation or maintenance of atrial fibrillation.

AIM: To observe the changes of sarcoplasmic reticulum Ca~(2+)-ATPase (SERCA), phospholamban (PLB) during heart failure after acute myocardial infarction (AMI) in rats and the effect of carvedilol. METHODS: Rats were randomly assigned to normal control group, sham-operation group, AMI group and carvedilol (CAR) group. 6 weeks later, in vivo hemodynamic, morphometry and SERCA, PLB mRNA and protein expression of myocytes were measured in all animals. RESULTS: In comparison with sham-operation group, LV end diastolic pressure (LVEDP) and weight of ventricles were increased, while maximal rate of rise and fall (?dp/dt) of LV pressure were decreased in AMI group. After treatment with carvedilol, these parameters were all improved. The mRNA and protein expression of SERCA were downregulated (P0.05). CONCLUSIONS: The changes of SERCA and PLB may be the important mechanism of contractile dysfunction in heart failure after AMI. Carvedilol is effective in preventing LV dysfunction after AMI. The molecular mechanism may be related with normalization of SERCA expression.

AIM: To investigate the electrophysiological changes of diabetic myocardium and effects of cyclovirobuxine D (CVB-D) on its electrophysiology. METHODS: Diabetes was induced in male SD rats, using a single injection of alloxan into tail vein. Untreated age-matched animals were used as controls. Animal electrocardiogram (ECG) was recorded by 2 weeks. Effects of CVB-D on isolated right ventricular papillary muscle from experimental diabetic rats and control group were observed by recording the transmembrane potentials with conventional glass microelectrodes. RESULTS: QT intervals in ECG and action potential duration (APD) at all levels were significantly lengthened in myocardium from week 2 of diabetes. Within the concentration of 13.3-63.3 ?mol?L~(-1), CVB-D prologated APD of diabetes in dose-dependent manner and more than that of control. Within the concentration of 33.3-63.3 ?mol?L~(-1), CVB-D depressed RP, APA, V_(max) and OS of diabetes in dose-dependent way and more than that of control. In addition, CVB-D at concentration of 20 ?mol?L~(-1) prologated APD in a time-dependent manner. The most prologation of APD was attained about 40 min in control, while more than 40 min in diabetes. CONCLUSION: The results show that QT intervals in ECG and APD at all levels are significantly lengthened in myocardium from week 2 of diabetes. CVB-D prolongates APD and inhibits RP, APA, OS and V_(max) more in diabetes than in control.

AIM: To investigate the effect of the heat shock response on the reperfusion arrhythmias(RAs) and the possible mechanism involved. METHODS: Fifty-five Sprague Dawley rats were randomly divided into 2 groups: the heat shock group (group H, n=29 ) and the control group (group C, n=26 ). The rats in group H were preconditioned with heat shock 24 hours before, and that in group C were not. The hearts of 16 rats in group H and 16 in group C were exercised and mounted on a non-circulating Langendorff perfusion apparatus and perfused retrogradely with modified K-H buffer and mimic ischemia/reperfusion was applied. Additionally, conventional intracellular microelectrode techniques were used for recording such electrophysiological parameters as resting potential(RP), action potential amplitude(APA), over shot(OS), maximum depolarization velocity(Vmax) of the hearts of other 13 rats in group H and 10 in group C. RESULTS: ①Prior heat stress significantly decreased reperfusion arrhythmia. ②The amount of CK release in the effluent in group H was much less than that in group C. ③Myocardial HSP70 content was elevated significantly in group H. ④Heat stress significantly increased myocardial anti-oxydases activity and decreased lipid peroxydative products. Additionally, heat stress significantly reduced the Vmax of action potential. It indicated that rapid Na + channel of papillary muscles may be inhibited by heat shock. The degree of change of Vmax after ischemia in H group was significantly less than that in group C. And the time of reperfusoin with Tyrode's solution till the action potential appeared as large as that before perfusion with mimic ischemic solution is shorter in group H than in group C. CONCLUSION: Heat shock pretreatment markedly reduces ischemia/reperfusion-induced injury of heart and ventricular arrhythmias in rats and this effect may be associated with the inhibition of rapid Na + channel of papillary muscles by heat shock and the increase in myocardial HSP70 and anti-oxydase activity.

AIM: To investigate the role of phosphoinositide pathway in the formation of pressure-overload cardiac hypertrophy. METHODS: Cardiac hypertrophy was induced in male Sprague-Dawley rats with coarctation of abdominal aorta, whole heart weight/body weight ratio was tested after 10 or 30 days of operation. Content of G?q/11 protein in left ventricle was detected by immunoblot analysis and concentration of IP 3 was measured by radioimmunoassay. RESULTS: At 10 and 30 days, whole heart weight/body weight ratio of coarctation aorta (CA) group was higher than that of sham-operated (SO) rats ( P 0.05). At 10 days, the level of IP 3 significantly increased in left ventricle of CA rats compared with the control animals ( P

Objective To explore the relationship between the extent of coronary artery lesions and plasma brain natriurefic peptide(BNP)levels in the patients with coronary artery disease(CAD)except for congestive heart failure(CHF).Method Seventy CAD patients without CHF evidenced by dinical manifestation and coronary arte- riography(CAG)from Cardiology Depamnent of the First Affiliated Hospital of Zhejiang University School of Medicine,China,were enrolled in the study.These patients were diagnozed under coronary arteriography(CAG) during March to May of 2007.They were divided into 3 groups:stable angina goup(24 patients),unstable angina group(25 patients),myocardial infarction group(21 patients).Twenty patients without coronary history and with normal CAG served as controls.Plasma BNP concentrations were measured with ELASA before CAG.The coronary lesion vessels and scores were estimated after CAG.The relationship between BNP levels and the coronary lesion vessels,as well as scores in CAD was analyzed.The data were expressed as(x±s)and was analyzed by using 2 independent samples test and spearman correlation with SPSS 13.0.A P value less than 0.01 indicated statistical significance.Results The plasma BNP concentrations in the patients,especially in the patients with myocardial infarction,were significantly higher than those in the controls.Spearman analysis showed that there was a positive correlation between the BNP levels and coronary lesion vessels(r1=0.309,P=0.01),also between BNP and coronary lesion score(r2=0.279,P=0.01).Conclusions In the patients without congestive heart failure,the more serious the coronary artery lesions,the higher the plasma BNP concentrations were.The degree of myocardial ischemia caused by coronary artery lesions was correlated with the plasma BNP level.Plasma BNP concentration could be valuable for the extent of coronary artery lesions in the patients of coronary artery disease.

AIM:To investigate the alterations of phospholamban(PLB)expression and cardiac sarcoplasmic reticulum(SR)Ca 2+-ATPase activity,and the change of cardiac function in rats with diabetes mellitus(DM).METHODS:The diabetes mellitus in male Wistar rats was induced by intraperitoneal injection of streptozotocin.The levels of PLB mRNA and PLB protein,the activity of SR Ca 2+-ATPase and the left ventricular hemodynamics parameters were measured 4 weeks,6 weeks and 8 weeks after DM was induced in rats,while the normal rats served as control group.RESULTS:There was no significant difference in PLB mRNA level and protein level between 4-week-DM rats and normal control rats.6-week-DM rats and 8-week-DM rats had markedly increased PLB mRNA and protein level compared with normal control rats.SR Ca 2+-ATPase activity was not significantly changed in 4-week-DM rats compared with normal control rats,and was markedly depressed in 6-week-DM rats and 8-week-DM rats.LVSP,LVEDP and ?dp/dt max were not significantly changed in 4-week-DM rats compared with normal control rats.In 6-week-DM rats and 8-week-DM rats,LVSP and ?dp/dt max were decreased,LVEDP was increased compared with normal control rats.CONCLUSION:The elevated levels of PLB mRNA and PLB protein contribute to SR Ca 2+-ATPase activity reduction,which leads to cardiac dysfunction in DM rats.

AIM: To explore the probable mechanisms of diabetes-induced arrhythmias. METHODS: Diabetes was induced in male SD rats,using a single injection of alloxan into tail vein. Untreated age-matched animals were used as controls. All animals were observed by 2,4,6 and 8 weeks,respectively. Transmembrane potentials were recorded with conventional glass microelectrodes. RESULTS: Action potential duration(APD) at all level (APD10,APD20,APD30,APD50,APD70,APD90) was significantly lengthened in right ventricular papillary muscle from week 2 of diabetes. At week 8,APD was more lengthened at any level of repolarization than that at week 2. No differences were observed in the maximum rate of depolarization(V_ max ),overshoot(OS) and action potential amplitude(APA) as well as the resting membrane potential(RP) from the 2th to 8th week of diabetes. CONCLUSION: The results indicate that prolongation of APD may be prominently responsible for the increased incidence of cardiac re-entry-arrhythmias and sudden death,especially at late stages of diabetes.